Department of Pediatrics, School of Medicine, Washington University in St Louis, Saint Louis, Missouri.
Birth Defects Res. 2018 Dec 1;110(20):1539-1550. doi: 10.1002/bdr2.1416. Epub 2018 Nov 14.
Maternal immune activation (MIA) refers to a maternal immune system triggered by infectious or infectious-like stimuli. A cascade of cytokines and immunologic alterations are transmitted to the fetus, resulting in adverse phenotypes most notably in the central nervous system. Epidemiologic studies implicate maternal infections in a variety of neuropsychiatric disorders, most commonly autism spectrum disorders and schizophrenia. In animal models, MIA causes neurochemical and anatomic changes in the brain that correspond to those found in humans with the disorders. As our understanding of the interactions between environment, genetics, and immune system grows, the role of alternative, noninfectious risk factors, such as prenatal stress, obesity, and the gut microbiome also becomes clearer. This review considers how infectious and noninfectious etiologies activate the maternal immune system. Their impact on fetal programming and neuropsychiatric disorders in offspring is examined in the context of human and animal studies.
母体免疫激活（MIA）是指母体免疫系统被感染或类似感染的刺激物触发。细胞因子和免疫改变的级联反应传递给胎儿，导致中枢神经系统出现不良表型，尤其是自闭症谱系障碍和精神分裂症。流行病学研究表明，母体感染与多种神经精神疾病有关，最常见的是自闭症谱系障碍和精神分裂症。在动物模型中，MIA 导致大脑的神经化学和解剖变化，与患有这些疾病的人类所发现的变化相对应。随着我们对环境、遗传和免疫系统之间相互作用的理解不断加深，非传染性危险因素（如产前应激、肥胖和肠道微生物组）的作用也变得更加清晰。这篇综述考虑了感染和非感染病因如何激活母体免疫系统。在人类和动物研究的背景下，探讨了它们对胎儿编程和后代神经精神疾病的影响。
